Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications
Abstract Background Acute myeloid leukemia (AML) is a rapidly progressing blood cancer. The prognosis of AML can be challenging, emphasizing the need for ongoing research and innovative approaches to improve outcomes in individuals affected by this formidable hematologic malignancy. Methods In this...
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2024-11-01
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| Series: | Journal of Translational Medicine |
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| Online Access: | https://doi.org/10.1186/s12967-024-05779-3 |
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| author | Yanli Chen |
| author_facet | Yanli Chen |
| author_sort | Yanli Chen |
| collection | DOAJ |
| description | Abstract Background Acute myeloid leukemia (AML) is a rapidly progressing blood cancer. The prognosis of AML can be challenging, emphasizing the need for ongoing research and innovative approaches to improve outcomes in individuals affected by this formidable hematologic malignancy. Methods In this study, we used single-cell RNA sequencing (scRNA-seq) from AML patients to investigate the impact of L-glutamine metabolism-related genes on disease progression. Results Our analysis revealed increased glutamine-related activity in CD34 + pre-B cells, suggesting a potential regulatory role in tumorigenesis and AML progression. Furthermore, intercellular communication analysis revealed a significant signaling pathway involving macrophage migration inhibitory factor signaling through CD74 + CD44 within CD34 + pre-B cells, which transmit signals to pre-dendritic cells and monocytes. Ligands for this pathway were predominantly expressed in stromal cells, naïve T cells, and CD34 + pre-B cells. CD74, the pertinent receptor, was predominantly detected in a variety of cellular components, including stromal cells, pre-dendritic cells, plasmacytoid dendritic cells, and hematopoietic progenitors. The study’s results provide insights into the possible interplay among these cell types and their collective contribution to the pathogenesis of AML. Moreover, we identified 10 genes associated with AML prognosis, including CCL5, CD52, CFD, FABP5, LGALS1, NUCB2, PSAP, S100A4, SPINK2, and VCAN. Among these, CCL5 and CD52 have been implicated in AML progression and are potential therapeutic targets. Conclusions This thorough examination of AML biology significantly deepens our grasp of the disease and presents pivotal information that could guide the creation of innovative treatment strategies for AML patients. |
| format | Article |
| id | doaj-art-3f36152e90d5401baf343ca61d03a79a |
| institution | Kabale University |
| issn | 1479-5876 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Translational Medicine |
| spelling | doaj-art-3f36152e90d5401baf343ca61d03a79a2024-11-10T12:40:57ZengBMCJournal of Translational Medicine1479-58762024-11-0122111510.1186/s12967-024-05779-3Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implicationsYanli Chen0The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer HospitalAbstract Background Acute myeloid leukemia (AML) is a rapidly progressing blood cancer. The prognosis of AML can be challenging, emphasizing the need for ongoing research and innovative approaches to improve outcomes in individuals affected by this formidable hematologic malignancy. Methods In this study, we used single-cell RNA sequencing (scRNA-seq) from AML patients to investigate the impact of L-glutamine metabolism-related genes on disease progression. Results Our analysis revealed increased glutamine-related activity in CD34 + pre-B cells, suggesting a potential regulatory role in tumorigenesis and AML progression. Furthermore, intercellular communication analysis revealed a significant signaling pathway involving macrophage migration inhibitory factor signaling through CD74 + CD44 within CD34 + pre-B cells, which transmit signals to pre-dendritic cells and monocytes. Ligands for this pathway were predominantly expressed in stromal cells, naïve T cells, and CD34 + pre-B cells. CD74, the pertinent receptor, was predominantly detected in a variety of cellular components, including stromal cells, pre-dendritic cells, plasmacytoid dendritic cells, and hematopoietic progenitors. The study’s results provide insights into the possible interplay among these cell types and their collective contribution to the pathogenesis of AML. Moreover, we identified 10 genes associated with AML prognosis, including CCL5, CD52, CFD, FABP5, LGALS1, NUCB2, PSAP, S100A4, SPINK2, and VCAN. Among these, CCL5 and CD52 have been implicated in AML progression and are potential therapeutic targets. Conclusions This thorough examination of AML biology significantly deepens our grasp of the disease and presents pivotal information that could guide the creation of innovative treatment strategies for AML patients.https://doi.org/10.1186/s12967-024-05779-3Acute myeloid leukemiaL-glutamine metabolismscRNA-seqDiagnosis model |
| spellingShingle | Yanli Chen Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications Journal of Translational Medicine Acute myeloid leukemia L-glutamine metabolism scRNA-seq Diagnosis model |
| title | Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications |
| title_full | Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications |
| title_fullStr | Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications |
| title_full_unstemmed | Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications |
| title_short | Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications |
| title_sort | dissecting l glutamine metabolism in acute myeloid leukemia single cell insights and therapeutic implications |
| topic | Acute myeloid leukemia L-glutamine metabolism scRNA-seq Diagnosis model |
| url | https://doi.org/10.1186/s12967-024-05779-3 |
| work_keys_str_mv | AT yanlichen dissectinglglutaminemetabolisminacutemyeloidleukemiasinglecellinsightsandtherapeuticimplications |